The in Vivo Radiosensitizing Effect of Magnolol on Tumor Growth of Hepatocellular Carcinoma

Background/Aim: Radiation (RT) induced ERK/NF-?B in hepatocellular carcinoma (HCC) has been reported in our previous works; it weakens the toxicity of RT or triggers a radioresistance effect. Thus, combining RT with a suitable NF-?B inhibitor may sensitize HCC to RT. Magnolol, a bioactive compound, was known to have antiinflammatory and anti-tumor functions. Here, we aimed to investigate whether magnolol may enhance anti-HCC efficacy of RT in vivo. Materials and Methods: We established a Hep3B bearing mouse to evaluate the efficacy of the combination treatment of magnolol and RT. Results: Most significantly, tumor volume and tumor weight inhibition was found in the combination group. Tumor immunohistochemistry staining also illustrated the suppression of RT-induced ERK/NF-?B-related proteins expression by magnolol. In addition, intrinsic apoptosis-related proteins, such as caspase-3 and-9, were markedly increased in the combination group. Conclusion: Magnolol may effectively enhance anti-HCC ability of RT by downregulating the expression of ERK/NFB-related proteins and increasing the expression of apoptosis-related proteins.